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Therapeutics II > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Empagliflozin non-diabetes FDA indications

A

Reduce risk of CV death (EMPA-REG trial)

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2
Q

Canagliflozin non-diabetes FDA indications

A

Reduce risk of MACE
Reduce risk of end-stage kidney disease, doubling of SCr, CV death, hospitalization for HF in patients with T2DM with neuropathy and albuminuria
CANVAS trial

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3
Q

Dapagliflozin non-diabetes FDA indications

A

Reduce risk of HF hospitalization in patients with T2DM and CVD or multiple CVD risk factors
Tx of heart failure with reduced ejection fraction in adults w/ or w/o T2DM
DECLARE-TIMI 58

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4
Q

Non-diabetes FDA indications for liraglutide, dulaglutide, and semaglutide

A

Reduce risk of MACE

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5
Q

Sulfonylurea MOA

A

sulfonylureas bind to the SUR1 receptor on pancreatic beta cells without the presence of glucose or ATP. This closes the ATP-dependent calcium channel opens the calcium channel and triggers insulin release

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6
Q

Sulfonylurea insulin effect

A

Mixed effect on FPB and PPG

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7
Q 
Glipizide 
Class: 
Brand: 
Dose:
Duration of action: 
Active metabolites?
A 
Class: Sulfonylurea
Brand: Glucotrol
Dose: 5-40mg QD-BID
Duration of action: Up to 20 hours
Active metabolites? No
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8
Q 
Glipizide ER
Class: 
Brand: 
Dose:
Duration of action: 
Active metabolites?
A 
Class: Sulfonylurea 
Brand: Glucotrol XL
Dose:5-20mg QD
Duration of action: 24 hours 
Active metabolites? No
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9
Q 
Glimepiride
Class: 
Brand: 
Dose:
Duration of action: 
Active metabolites?
A 
Class: Sulfonylurea
Brand: Amaryl
Dose: 1-8mg QD
Duration of action: 24 hours
Active metabolites? No
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10
Q

Why are most sulfonylureas QD?

A

Because most of them have a 24 hour onset of action

Sometimes dosed BID because this decreases the peak effect which decreases the risk of hypoglycemia

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11
Q

Sulfonylureas AE

A 
Hypoglycemia
Weight Gain (sulfonylureas promote the release of insulin which is an anabolic hormone and it builds up fat and protein and allows for more glucose to enter the cells)

Less common: rash, photosensitivity, dyspepsia, nausea, HA

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12
Q

Sulfonylureas contraindications

A

Hypersensitivity
DKA
Type 1 Diabetes
H/O allergic reaction to sulfonamide derivatives (glimepiride)
Concomitant administration of bosentan (glyburide)

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13
Q

Sulfonylureas advantages/disandvantages

A

Advantages- quick onset, high initial response rate, inexpensive
Disadvantages- hypoglycemia, weight gain, high secondary failure rate (5-10%/year)

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14
Q

Sulfonylureas DDI

A

CYP2C9

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15
Q

Do you titrate sulfonylureas?

A

Yes, to minimize the AE if hypoglycemia and to reach target dose

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16
Q

Why is there a high secondary failure rate with sulfonylureas?

A

Because their activity depends on active, functional beta cells and we lose beta cell mass and function at a rate of 5-10%/year

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17
Q

Meglitinides (Glinides) MOA

A

Similar MOA to sulfonylurea, the binding site is adjacent.

Difference- requires presence of glucose so hypoglycemia is less common

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18
Q

Meglitinides (Glinides) medications and where they effect BG

A

Repaglinide, Nateglinide- both rarely used because they are dosed TID before meals so adherence is poor.

Requires glucose so they effect the PPG

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19
Q

Meglitinides (Glinides) adverse effects and contraindications

A

AE: hypoglycemia and weight gain
Contraindications: hypersensitivity, DKA, T1DM, Repaglinide with gemfibrozil

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20
Q

Meglitinides (glinides) advantages/disadavantages and metabolism

A

Advantages- Rapid onset of action, less AE than sulfonylureas, postprandial glucose
Disadvantages- hypoglycemia, weight gain, secondary failure (MOA depends on a functional beta cell), and TID dosing

Metabolism- CYP2C8 (DDI with repaglinide and TMP)

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21
Q

Biguanide (metformin) MOA

A

Primary effect on the liver, it inhibits gluconeogenesis (production of glucose from noncarbohydrate precursors)
Secondarily causes improvement on peripheral insulin resistance

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22
Q

Metformin dose/brand name

A

Glucophage or Glucophage XR
Dose titration to decrease the AE of diarrhea until maximum dose of 2,550mg/day.
Titrate by increments of 500mg at biggest meal of the day
Even glucophage XR is split into BID dosing to minimize peak effects and decrease AE

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23
Q

What BG does metformin effect?

A

FPG because the liver is the primary source of glucose in the fasting state

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24
Q

Metformin AE

A

Common: N/V/D (Diarrhea most common), these effects are transient and will go away with continued use
Uncommon: macrocytic anemia

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25
Q

Metformin contraindications and BBW

A

Hypersensitivity
eGFR <30mL/min
Active chronic metabolic acidosis

BBW- lactic acidosis

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26
Q

Metformin warnings/precautions

A

Starting metformin in patients with a eGFR 30-45mL/min is not recommended
IV contrast-induced nephropathy
Hypoxic states (renal failure, liver failure, HF, pulmonary failure increase lactate)
Severe hepatic/pulmonary disease

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27
Q

Cori cycle

A

Causes an increase in lactate through backup processes. In anaerobic conditions we could see an increase in lactate, contributing to metformin- induced lactic acidosis

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28
Q

Metformin advantages/disadvantages and DDI

A

Advantages- no hypoglycemia as monotherapy (it does not increase the release of insulin), weight neutral or loss, high initial response rate, positive lipid effects (decrease LDL, TG and increases HDL), inexpensive

Disadvantages- GI AE (take WF to help)
DDI-cimetidine

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29
Q

Thiazolidinediones MOA

A

Increases insulin sensitivity
Secondarily decreases hepatic glucose production
PPAR-y agonist

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30
Q

Thiazolidinediones adverse effects

A 
Weight gain (glucose enters cell)
Fluid retention (increased incidence with insulin)
HF exacerbation 
Fractures
Hepatotoxicity
Bladder cancer
Macular edema
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31
Q

Pioglitazone

A

Thiazolidinedione
15-45mg QD titrated to therapeutic response
Delayed onset of action so the maximal effect is seen in 8-12 weeks
Mixed effect, but primarily FPG

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32
Q

Thiazolidinediones contraindications

A

NYHA Class III and IV HF

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33
Q

Thiazolidinedione advantages and disadvantages

A

Advantages- No hypoglycemia as monotherapy, favorable lipid effects (increase HDL, decrease TG), can use in renal in sufficiency
Disadvantages- delayed onset of action, several potential AE, recommend LFT monitoring

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34
Q

Thiazolidinedione DDI

A

Gemfibrozil w/ pioglitazone

Max dose of pioglitazone 15mg/day

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35
Q

alpha-glucosidase inhibitors MOA

A

Prevents breakdown of complex carbohydrates into glucose, delaying and reducing post-meal carb absorption and post prandial BG rise.
Must take WF since it inhibits the breakdown of complex carbs.

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36
Q

alpha-glucosidase inhibitors meds and glucose effect

A

acarbose and miglitol
Both dose titrated
Effect on PPG

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37
Q

alpha-glucosidase inhibitors adverse effects

A

Common (directly related to carbs not be digested)- flatulence, abdominal discomfort, diarrhea

Rare- LFT elevation (acarbose)

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38
Q

alpha-glucosidase inhibitors contraindications and warnings/precautions

A

Contraindications- hypersensitivity, DKA, cirrhosis, IBD, colonic ulceration, intestinal obstruction

warnings/precautions- SCr >2mg/dL

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39
Q

alpha-glucosidase inhibitors advantages/disadvantages

A

Advantages- no hypoglycemia as monotherapy, weight neutral

Disadvantages- modest efficacy, poorly tolerated GI AE, slow titration, multiple doses/day so poor adherence

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40
Q

DPP-4 inhibitors MOA

A

DPP4 inactivates or breaks down the incretin hormones (GLP-1 and GIP-1)
The incretin hormones come from the intestines (L cells) and you see a bigger rise after a meal.
In T2DM, you have a decrease in incretin hormones and DPP-4 inhibitors prevent the breakdown of your bodies own GLP-1

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41
Q

What does GLP-1 do?

A

Gut- delays gastric emptying
Liver- suppresses glucagon secretion
Pancreas- increases insulin release
1- 1 brain- suppresses appetites, increases satiety

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42
Q

What BG do DPP-4 inhibitors effect?

A

PPG because they only work in the presence of glucose. DPP-4 inhibitors are only around when GLP-1 is around which is when you’re eating

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43
Q 
Sitagliptin 
Class: 
Brand: 
Dose:
A1C lowering monotherapy:
A1C lowering combo therapy:
Renal dosing:
A 
Class: DPP-4 inhibitor
Brand: Januvia
Dose: 100mgQD
A1C lowering monotherapy- 0.6%
A1C lowering combo therapy- 0.7%
Renal dosing:
50mg QD when CrCl 30-50mL/min
25mg/day when CrCl <30mL/min
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44
Q 
Linagliptin
Class: 
Brand: 
Dose:
A1C lowering monotherapy:
A1C lowering combo therapy:
Renal dosing:
A 
Class: DPP-4 inhibitor
Brand: Tradjenta
Dose: 5mg QD
A1C lowering monotherapy: 0.4%
A1C lowering combo therapy: 0.7%
Renal dosing: N/A
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45
Q

DPP-4 inhibitors AE and drug interactions

A

AE- nasopharyngitis (runny nose), URI, HA.
Very well tolerated

DDI- CYP3A4

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46
Q

DPP-4 inhibitors contraindications, warnings and precautions

A

Contraindications- hypersensitivity

Warnings/Precautions- pancreatitis, HF, arthralgia (goes away if you D/C)

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47
Q

DPP-4 inhibitors advantages/disadvantages

A

Advantages- No hypoglycemia as monotherapy, weight neutral

Disadvantages- expensive

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48
Q

Bile acid sequestrants MOA and medication

A

Inhibits bile acid reabsorption leading to a decrease in hepatic glucose production
Colesevelam- tk with food

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49
Q

Bile acid sequestrants AE, contraindications, DDI

A

AE- constipation

contraindications (all because of constipation)- H/O bowel obstruction, TG >500mg/dL, H/O TG-induced pancreatitis

DDI- separate other drugs by 4 hours

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50
Q

Bile acid sequestrants advantages/disadvantages

A

Advantages- No hypoglycemia as monotherapy, LDL lowering of 15-18%, may increase metformin tolerability
Disadvantages- Modest A1C lowering, high pill burden, may raise TG

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51
Q

Dopamine agonist (Bromocriptine) MOA, effects which BG

A

Unknown
Increases EPI/NE to improve insulin sensitivity in the liver
Effect PPG

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52
Q

Dopamine agonists (Bromocriptine) AE and contraindications

A

AE- GI and CNS (N/V, asthenia, constipation, dizziness, somnolence)
Contraindications- hypersensitivity to ergot derivative, lactation, syncopal migraines

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53
Q

Dopamine agonists (bromocriptine) advantages/ disadvantages/ DDI

A

Advantages- unique MOA
Disadvantages- modest efficacy, AE, cost
DDI- CYP3A4, protein-binding, drug-disease

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54
Q

SGLT2 inhibitors MOA

A

In T2DM, you see an upregulation of SGLT2. SGLT2 inhibitors inhibit the reabsorption of glucose and glucose gets eliminated in the urine

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55
Q

SGLT2 effects which BG?

A

It effects both FPG and PPG and has a low risk of hypoglycemia

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56
Q

Canagliflozin
Brand
Dosing Renal dosing

A

Brand- Invokana
Dosing- 100-200mg daily (can titrate up from lower dose or start from higher one)
Renal dosing- Not recommended if GFR <45
If GRF 30-45 +UACR >300= 100mg daily

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57
Q

EMPA-REG outcome

A

Empagliflozin gets approved for reduce the risk of CV events

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58
Q

CANVAS trial

A

Canagliflozin gets approved for reduce risk of CV events

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59
Q

DECLARE-TIMI 58

A

Dapagliflozin gets approved to reduce risk of HF hospitalization in patients with T2DM and CVD or multiple CVD risk factors

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60
Q

VERTIS CV

A

Ertugliflozin has no heart benefits

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61
Q

SGLT2 inhibitors AE

A 
Hypotension (bc of water loss)
Hyperkalemia
Genital mycotic infections
UTI
Increased urination
Euglycemic DKA (why we shouldnt use in T1)
Bone fractures (canagliflozin)
AKI
Bladder cancer (dapagliflozin)
Leg/foot amputations
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62
Q

SGLT2 inhibitors contraindications

A

Hypersensitivity
Severe renal impairment
ESRD
Dialysis

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63
Q

SGLT-2 inhibitors advantages/disadvantages

A

Advantages- unique MOA, no hypoglycemia as monotherapy, weight loss, decrease in SBP
Disadvantages- AE, cost

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64
Q

Warning for all SGLT2 inhibitors

A

Necrotizing fasciitis of the perineum (fourniers gangrene), rare-life threatening bacterial infection

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65
Q

How do SGLT2 inhibitors help with HF?

A

Normally, the SGLT2 inhibitor causes Na and Glucose to be reabsorbed and K to be wasted in the urine.
With a SGLT2 inhibitor, Na, glucose, and water are all wasted in urine.
Consequently, hyperkalemia is possible bc it is being retained

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66
Q

Euglycemic DKA

A

When BG is normal but a patient still has DKA
when insulin decreases, lipolysis and glucagon increases, this leads to FFA formation which gets broken down into ketones

Look for N/V and abdominal pain

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67
Q

CREDENCE

A

Canagliflozin
FDA approval to reduce risk of ESRD, double of SCr, CV death, and hospitalization in HF for pts with T2DM and diabetic nephropathy with albuminuria

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68
Q

DAPA-CKD

A

Dapagliflozin shown to have positive benefits on CKD progression

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69
Q

DAPA- HF

A

Dapagliflozin
50% pts with diabetes and 50% w/o
Showed benefit in patients with HF

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70
Q

EMPEROR-reduced

A

Empagliflozin

statistically significant results in HF and decrease risk of CV death

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71
Q

How do SGLT2 inhibitors regulate tubuloglomerular filtration?

A

Normally, the SGLT2 channel reabsorbs Na and glucose and the rest of the Na gets sent to macula densa which causes the macula densa to sense Na.
In T2DM, there is a hyperfiltration that causes more glucose to be reabsorbed so there is less Na in the macula densa. This tells the body to filter faster causing a progression of CKD.
SGLT2 inhibitors cause more Na to be sent to the macula densa which regulates tubuloglomerular filtration

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72
Q

Amylin analog MOA, drug, BG effects

A

MOA- amylin is cosecreted with insulin in the beta cell in normal people
Amylin analogs cause synthetic amylin to be secreted which suppresses high postprandial glucagon secretion, increases satiety, and slows gastric emptying
Drug- Pramlintide -for type 1 and 2 DM (Different doses)
Effects PPG so must be administered with meals (lower dose of meal time insulin

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73
Q

Amylin analog adverse effects, contraindications, and warnings/precautions

A

Adverse effects- N/V, hypoglycemia with insulin (BBW)
Contraindications- hypersensitivity, gastroparesis, unawareness of hypoglycemia

Warnings/precautions- A1C >9%, patients unwilling to SMBG

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74
Q

Amylin analog advantages/disadvantages

A

Advantages- weight loss

Disadvantages- additional injections, may reduce rate and absorption of drugs because of delayed gastric emptying, GI AE

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75
Q

GLP-1 receptor agonists MOA

A

Synthetic analog of GLP-1
GLP-1 decreases gastric emptying, decreases glucose production, causes the pancreas to release insulin, and increases satiety
Glucose dependent

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76
Q 
Liraglutide
Class
Brand
Dosing
Administration
Delivery
Storage
Renal dosing
A 
Liraglutide
Class- GLP-1 receptor agonist
Brand- Victoza
Dosing- 0.6mg SQ daily, titrate weekly to 1.2mg and 1.8mg if tolerated
Administration- independent of meals and time of day
Delivery- Pen
Storage- Room temp for 30 days
Renal dosing- NA
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77
Q

Which GLP1 receptor agonists do you have to renal dose?

A

Exenatide and Exenatide XR

Not recommended with CrCl <30

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78
Q

Lixisenatide (Adlyxin)

A

ELIXA trial- neutral effect on CV outcomes

Non-human based GLP1 receptor agonists

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79
Q

Semaglutide (Ozempic)

A

Titrated with 3 doses, first therapeutic dose at 0.5
GLP1 receptor agonist, administor any time of the day with or without meals
Long carbon fatty acid chain is why it has weekly doses

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80
Q

Oral semaglutide

A

Only oral GLP1 agonist
Rybelsus
PIONEER 6- neutral effect of CV outcomes
co-formulated with SNAC so that the medication gets attached to one area of the stomach
Have to take 30 minutes before eating, drinking, or taking any other medications. Take with no more than 120mL water

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81
Q

LEADER

A

Liraglutide decreases risk of major CV events

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82
Q

EXSCEL

A

Exenatide- no significant CV benefits

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83
Q

REWIND

A

Reduce risk of major CV events

Dulaglutide

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84
Q

SUSTAIN-6

A

Semaglutide

Decrease risk of CV events

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85
Q

GLP1 receptor agonists AE, contraindications, BBW

A

N/V/D (Nausea most common)
Injection site reactions or nodules (bydureon)
Contraindications- hypersensitivity, personal or family history of medullary thyroid carcinoma, patients with MEN 2

BBW- risk of thyroid C-cell tumors

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86
Q

GLP1 receptor agonists advantages and disadvanteges

A

Advantages- weight loss, convenient dosing

Disadvantages- May reduce rate and absorption of drugs, injections/training, must stay hydrated or prerenal AKI possible

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87
Q

Xultophy

A

Insulin degludec and liraglutide
QD injection
Dose range 10-50

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88
Q

Soliqua

A

Insulin glargine and lixisenatide

Administer 1 hr before 1st meal of day

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89
Q

Insulin pharmacology

A

Insulin is a protein that is made up of AA. It comes from proinsulin.
If you make insulin, you also make C-Peptide.
It is stored in crystals (hexamers around a zinc molecule) and degraded in the liver and kidneys.
Half life of 3-5 minutes

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90
Q

Rapid acting insulin

A

Insulin lispro (Humalog)
Insulin aspart (Novolog)
Insulin glulisine
(Admelog is similar but not approved to be bioequivalent)

-All insulin analogs , which are predictable! The have the lowest variability of absorption (5%).
Stabilized into hexamers by a cresol preservative. Rapid-acting insulin rapidly goes from hexamer to monomer form for diffusion.
Take about 15-20 minutes before a meal.

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91
Q

Fiasp

A

Faster acting insulin aspart
Ultra-rapid acting (has a 10 minute earlier onset of action than the rapid acting insulins)
Contains niacinamide (Vit B3 as an excipient that increases the absorption)
Inject at the start of a meal or within 20 minutes after starting a meal. Allows for more variability in timing.

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92
Q

Lyumjev

A

Faster acting insulin lispro
Comes in 100 and 200 units/ml
Excipients:
citrate- increases vascular permeability
Treprostinil- increases local vasodilation
Both allow for a quicker absorption
Administration- inject at the start of a meal or within 20 minutes after starting a meal

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93
Q

Inhaled insulin

A

Afrezza (human insulin, ultrarapid acting)
Acts more like a rapid acting analog
Indications- T1DM or T2DM adult, must be used with long-acting insulin if used in T1DM, not recommended for DKA or smokers
Contraindications- chronic lung disease, asthma, COPD
Warnings- decline in pulmonary function, lung cancer
Need to measure FEV1 and respiratory function
BBW- acute bronchospasm in patients with asthma/COPD

Meal time insulin

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94
Q

Afrezza storage

A

Inhaler- good for 15 days

cartridges- good for 10 days at RT when sealed, 3 days when opened

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95
Q

Afrezza dosing

A

Use a 1.5x conversion
limited to 4, 8, or 12 units
You need more afrezza than your typical meal time insulin
Injected meal time insulin 5-8 units, afrezza dose 8units

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96
Q

Short-acting insulin

A

Regular insulin (human)
Self-aggregate in antiparallel fashion to form dimers and then stabilize around zinc ions to create hexamers
When injected it gets diluted by the interstitial fluid and goes from hexamers to dimers to monomers. It undergoes the dimer step to increase the onset of action.
Human insulin so variability in dose and PK/PD profile.
Because of the slower onset of action, must be given 30 minutes prior to a meal.

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97
Q

1st phase release of insulin

A

Insulin-independent GLUT2 receptor on the beta cell causes the calcium channel to open and insulin to be released.
Insulin is stored in the beta cell (this is messed up in T2DM)

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98
Q

Phase 2 release of insulin

A

Insulin meets the insulin receptor and undergoes a network of phosphorylation’s that activate the GLUT4 (insulin dependent) receptor. GLUT4 (on muscles and adipose tissues) then accepts glucose into the cell to become metabolized

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99
Q

Where does insulin come from?

A

Beta cells
Synthetic insulin used to come from beef and pork sources but we dont use this anymore due to impurities
We use recombinant insulin made from bacteria and yeast

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100
Q

Human insulin vs. insulin analogs

A

Human insulin is any insulin, regardless of if you make it yourself, that has the same AA structure as the insulin we make in our own bodies,

Insulin analogs have AA switches that change the PK/PD effects.

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101
Q

Human insulin examples

A

Insulin glargine
Regular insulin
NPH

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102
Q

Insulin analogs examples

A

Insulin lispro
Insulin aspart
Insulin detemir
Insulin glulisine

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103
Q

Humulin R U-500

A

Typically reserved for patients requiring more than 200units/day of insulin which indicates insulin resistance.
Very dangerous so be extra sure that patient understands and uses correct syringe.

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104
Q

Intermediate-acting insulin

A 
NPH insulin (human insulin)
Novolin R or Humulin R
Combination of insulin and protamine to increase duration of action. After injection, proteolytic tissue enzymes have to degrade protamine bound to the insulin hexamers before the insulin can be broken down into the dimer and monomer forms.

Insulin is cloudy due to the protein, do not shake but roll in hands

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105
Q

Long-acting insulin

A

Insulin glargine (Lantus) is soluble in acidic solutions so once it goes into the neutral bodies pH it precipitates into a crystalline depot. Individual insulin molecules slowly break away. Basaglar is also insulin glargine but they are not interchangeable.

Insulin detemir- self-aggregates due to albumin binding. Dose dependent profile (<0.3units/kg= BID, >0.3units/kg=QD)

Insulin degludec- multiple hexamer formation resulting in a SQ depot. It has reversible albumin binding.

106
Q

Toujeo

A

Insulin glargine U-300 (concentrated long acting insulin)
Need 10% more Toujeo to meet needs, we dont know why.
1.5mL SoloStar or 3mL Max SoloStar

Indications: glycemic control in diabetes mellitus, not used for DKA

Can cause hyper or hypo glycemia with changes in insulin regimen
Only comes in a prefilled pen

107
Q

Tresiba

A

Insulin degludec
U-100 or U-200 FlexTouch

Longest duration of action (42 hours). Builds into multihexamers once injected which causes this long DOA.
Dose daily at any time of the day
Allow for 3-4 days before dose increases
Allow a minimum of 8 hours between consecutive injections

108
Q

Insulin stacking

A

Increases risk of hypoglycemia
We are worried about this in the shorter acting insulins
With longer acting insulin we do not worry because they reach steady state in a few days

109
Q

Premixed insulin

A

Typically reserved for patients who have cost issues or will not take more than 2 injections per day.
%70/30= 70% NPH (bound to protein)/ 30% regular insulin (not bound)

Give at breakfast and dinner

110
Q

Which insulin is given IV?

A

Regular insulin

111
Q

Which insulins have a duration over 24 hours?

A

U-300 glargine and degludec

112
Q

Which insulins have a duration under 5 hours?

A

Technosphere, glulisine, lispro, aspart

113
Q

Which insulin has a duration between 4-6 hours?

A

Regular insulin

114
Q

Which insulin has a duration between 8-12 hours?

A

NPH

115
Q

Which insulins have a duration between 14-24 hours?

A

Detemir

Glargine (U-100)

116
Q

Insulin adverse effects

A

Hypoglycemia is the most common
Weight gain (insulin is anabolic and builds up fat and protein)
Injection site reactions (not as common)

117
Q

Hypoglycemia

A

Typically BG <70mg/dL
S/S- Tremor, diaphoresis (sweating), lightheaded, HA, tachycardia, nervous/anxious, irritable, confusion, hunger, drowsiness
Use the Rule of 15 to treat hypoglycemia- consume 15g of simple carbohydrates (orange juice, glucose tablets) and retest in 15 minutes. Retest until BG is normalized.

118
Q

Hypoglycemic unawareness

A

Loss of warning signs and S/S of hypoglycemia

119
Q

What are the 5 counterregulatory hormones and what do they do?

A

They increase BG

Glucagon, Epi, NE, Cortisol. GH

120
Q

When do you start seeing severe symptoms of hypoglycemia?

A

BG under 40

121
Q

Hypoglycemia level 1

A

Glucose 54-70mg/dL

122
Q

Hypoglycemia Level 2

A

Glucose <54mg/dL

123
Q

Hypoglycemia Level 3

A

A severe event characterized by altered mental and/or physical status requiring assistance.

124
Q

Glucagon

A

For adults and children over 6 years old-
1mg (1mL) IM repeat in 15 minutes if needed

For children <6
-0.5mg (0.5mL) IM repeat in 15 minutes if needed

Place patient on side in position to avoid aspiration from vomit and call 911.

125
Q

Gvoke and GvokeHypoPen

A

SQ preconstituted glucagon administration
For ages >2
Works like an epipen

126
Q

Glucagon nasal powder

A

For ages 4 and up

127
Q

Basal insulin

A

The insulin that your body produces at all times regardless of carb intake

128
Q

Prandial insulin

A

The insulin that your body produces after meals

129
Q

Treatment for T1DM

A

Patients should be treated with multiple daily injections
Pick either
-Basal and prandial injections
-Continuous subcutaneous insulin infusion

Most patients should be educated in matching prandial insulin dose to carbohydrate intake, premeal blood glucose, and anticipated activity.

Insulin analogs are preferred

130
Q

Total Daily Dose

A

For a new diagnosis begin with 0.5units/kg/day.
This will be adjusted for patient-specific needs
Insulin needed for entire day

131
Q

Basal-bolus dosing

A

Step 1:
Calculate TDD (insulin needed for entire day)
Step 2:
Split this dose in half. 50% will go to basal dose (NPH or long acting insulin) and 50% will be given before each meal (this 50% is divided by 3 and is given via rapid acting insulin or ultra rapid acting insulin)

132
Q

Split-mixed dosing

A

2 injections/day
Calculate TDD and then split into 1/3rds.
2/3rds of TDD will be given in the morning to account for breakfast and lunch
1/3rd given at night to account for dinner. Less given at night to prevent hypoglycemia while sleeping.

133
Q

Continuous subcutaneous insulin infusion

A

Uses rapid acting insulin
Mainly aspart (novolog) or lispro (humalog)
Typically given at the patients basal rate (0.5units/kg/hour)

134
Q

Correction Factor

A

Also called insulin sensitivity
Calculated to estimate the approximate plasma glucose lowering effect of 1 unit of short-acting insulin.
Example: If you correction factor is 50 then 1 unit of insulin will lower your BG by 50mg/dL
Corrects premeal glucose

135
Q

How do you calculate correction factor?

A

Regular insulin- 1500/TDD

Most common** Rapid acting- 1700/TDD

136
Q

How to calculate meal-time insulin doses

A

1.) Initial TDD is an estimate, it will be adjusted. Once we understand the patients true TDD we will move on to carb counting.
2.) 50% TDD is basal and 50% is prandial
Divide the 50% prandial insulin into 3 and give at
each meal. Calculate the correction factor for the
patient (1700/TDD) and add insulin based off of the
correction factor. Goal glycemic range is 80-
130mg/dL.

137
Q

How do you make a correction factor scale?

A

Goal is 80-130mg/dL
Anything less than 80mg/dL, you subtract 1 unit from the dose.
The CF is then used to make the scale. If the correction factor was 30 then every 30 mg increase in BG you give 1 extra unit of insulin

138
Q

Carbohydrate counting

A

Very effective
Use I:CHO ratio
Example- if your I:CHO ratio was 15 then 1 unit of insulin will cover 15 grams of carbs. If you are eating 30 carbs you would give 2 units of insulin.
Calculation:
Rule of 500-
500/TDD= I:CHO ratio for rapid-acting insulin
450:TDD= I:CHO ratio for regular insulin (less common)

139
Q

Insulin management priority list

A

Keep BG between 80-130mg/dL

  1. ) Target lows first
  2. ) Look at FPG and fix next
  3. ) Look for a 3-4 day pattern in the glucose log
  4. ) Identify the insulin dose that is responsible for the increase or decrease in BG
  5. ) Adjust this dose by 10-20%

Only adjust 1 dose at a time and then look for a new pattern.

140
Q

Pre-breakfast BG value is caused by what?

A

Meal- Dinner/bedtime
Insulin-
Basal-bolus- Bedtime (long-acting)
split-mixed- (Pre-dinner NPH)

141
Q

Pre-lunch BG value is caused by what?

A

Meal- Breakfast
Insulin-
Basal-bolus and split mixed- pre-breakfast insulin (rapid-acting)

142
Q

Pre-dinner BG value is caused by what?

A

Meal-lunch
Basal-bolus- Pre-lunch dose (rapid acting insulin)
Split-mixed- pre-breakfast dose (NPH)

143
Q

Bedtime BG value is caused by what?

A

Meal- Dinner
Insulin-
Basal-bolus- Pre-dinner insulin (rapid acting)
Split mixed- (Pre-dinner insulin (rapid acting)

144
Q

How does physical activity affect insulin?

A

Causes hyperglycemia due to “fight or flight” response caused by NE or EPI
Causes hypoglycemia due to the overexpression of the GLUT1 (insulin dependent) receptor. This increases the sensitivity of this receptor for 7-11 hours postexercise.

145
Q

Recommendations to decrease risk of hypoglycemia with exercise

A 
Make sure preexercise BG is >100mg/dL
Increase food intake
Reduce prandial insulin
Reduce overnight basal insulin
SMBG PRN
Simple carbs
146
Q

Potential risks of hyperglycemia

A 
Underestimating carb intake
High fat meal
Missed/inadequate medication doses
Ineffective insulin
Poor administration technique
Overuse of injection site
Less than usual activity
medications 
Illness, pain, stress
147
Q

Potential causes of hypoglycemia

A 
Irregular timing of medications
Incorrect medication dosing
Overestimation of carb intake
Skipping/delaying meals
More than usual activity
Decreased insulin needs (weight loss, increased physical activity)
148
Q

Lipohypertrophy

A

Build up of fat tissues because of insulin administration.
Need to rotate injection sites
Patients with this might need to increase insulin doses due to insulin not being absorbed

149
Q

Dawn phenomenon

A

When hormones are released in the mornings because they have different cycles. You need to check overnight insulin to determine if hypoglycemia is in?caused by the dawn phenomenon

150
Q

Which injection site has the most rapid absorption of insulin?

A

Abdominal fat

151
Q

Hybrid closed loop system

A

Medtronic and T:slim
CGM
insulin pump with tubing

152
Q

Control-IQ technology

A

CGM with no tubing

153
Q

Sick day management

A 
Continue basal insulin at normal dose
If not eating:
D/C premeal insulin and cover hyperglycemia with rapid-acting insulin Q 4-6 hours
Stay hydrated
Monitor every 1-2 hours
Check ketones every 4 hours if BG>250

Call MD if vomiting and BG >500 or moderate urine ketones

154
Q

Prediabetes recommendations

A

Intensive behavioral lifestyle intervention programs
Achieve and maintain 7% loss of initial body weight
Moderate intensity exercise to at least 150min/week

Annual monitoring

Metformin 850mg BID should be used if
BMI>35
Age <60
H/O GDM

155
Q

Pharmacotherapy for T2DM

A

Metformin preferred
Consider initiating insulin therapy if newly diagnosed, symptomatic, A1C >10% and/or BG >300mg/dL
Consider initiating dual therapy in newly diagnosed pts if A1C is 1.5-2% above target

In most patients, GLP-1 RA are preferred over insulin

156
Q

Youth-onset T2DM

A

3 approved drugs- insulin, metformin, liraglutide

If insulin targets are not met with metformin +/- basal insulin in children over 10 add liraglutide

157
Q

What do you give to T2DM patients who are on metformin and have ASCVD

A

GLP-1 RA with proven benefit (Liraglutide, Dulaglutide, Semaglutide)
OR
SGLT-2 inhibitor with CVD benefit (Empagliflozin, Canagliflozin)

If A1C still above target:
For patients on GLP-1 RA add SGLT2 inhibitor
Add Dpp-4 if not on GLP-RA
Basal insulin
TZD
SU
158
Q

What do you glve to T2DM patients who are on metformin and have HF or CKD

A

SGLT2 with evidence if GFR adequate (Dapagliflozin, Canagliflozin, Empagliflozin)
OR
Only if SGLT2 cant be used give GLP1-RA with proven CV benefits (Liraglutide, Dulaglutide, Semaglutide)

If A1C still above target:
For patients on  SGLT2 inhibitor consider GLP1 RA
Add Dpp-4 if not on GLP-RA
Basal insulin
SU
159
Q

What do you give T2DM patients if cost is a major issue?

A

SU or TZD

160
Q

What do you give T2DM patients who need to lose weight?

A

GLP1-RA or SGLT2

161
Q

What do you give in T2DM patients who need to minimize hypoglycemia?

A

DPP4
GLP1-RA
SGLT2i
TZD

162
Q

When do you add insulin to a T2DM patient?

A

If not meeting goals and already on GLP1-RA or GLP1-RA not tolerated add basal insulin
Start at 10IU/day or 0.1-0.2units/kg/day

163
Q

How do you titrate basal insulin for T2DM?

A

Start at 10IU/day or 0.1-0.2units/kg/day

10-20% every 2-3 days

164
Q

What do you do if T2DM patient is on basal insulin and not meeting goals?

A

Add prandial insulin
One dose with largest meal of day
Initiation- 4U a day or 10% of basal dose
Titrate by 1-2 IU or 10-15% twice weekly

165
Q

What to do if A1C above target in T2DM patients and patient is on basal and prandial insulin correctly titrated

A

Stepwise additional injections of prandial insulins and potentially proceed to full basal-bolus insulin
Consider split mixed regimen
Consider twice daily premixed insulin

166
Q

Critical point for basal insulin T2DM

A

0.5units/kg or higher we worry about over-basalization of increasing basal doses. So the increasing basal doses are not working as effectively and you might need them

167
Q

Stress hyperglycemia

A

Illness can cause hyperglycemia by increasing stress hormones (cortisol and EPI)
Hyperglycemia can lead to organ failure, sepsis, and death

168
Q

Hyperglycemia in hospitalized patients

A

Any BG >140mg/dL
BG levels that are consistently above this may require treatment
A1C >6.5% suggests that diabetes preceded hospitalization

169
Q

Critically ill patients (ICU) with hyperglycemia

A

IV insulin when BG gets between 140-180mg/dL
Maintain a BG target of 140-180mg/dL
Never let BG get below 110
Insulin infusion protocols are highly recommended

170
Q

Noncritically ill patients with hyperglycemia in hospital

A

Maintain BG target of 140-180mg/dL

Scheduled SQ insulin that delivers basal, nutritional, and correction components recommended

171
Q

Oral antihyperglycemics in the hospital

A

Limited data
Concerned because of long duration of action of agents, NPO, limited oral intake, and alternative nutrition therapies (TPN)

172
Q

IV insulin dosing in hospital

A

Protocols in specific hospitals determine rate

1unit/mL in 0.9% NaCl

173
Q

Basal-bolus regimen in hospitalized patients

A

Preferred method in non-ICU patients

  1. ) Determine the basal dose (Take 2/3rd of the total dose given in the ICU)
  2. ) Determine TDD (basal dose x2)
  3. ) Bolus insulin dose. These patients are eating very little so give 10% of basal dose for each meal. This will increase as the patient starts eating more.
  4. ) Correction scale measurement based off of patients CF.
174
Q

Hypoglycemia triggers in hospitalized patients

A 
Sudden reduction in corticosteroid dose
Altered ability to report symptoms
Reduced oral intake
Emesis
New NPO status
Inappropriate timing of insulin
Reduced infusion rate of dextrose
Unexpected interruption in TPN or parenteral infusions
175
Q

Hypoglycemia protocol if patient can take PO

A

BG <70 stop insulin
If BG 50-70 start rule of 15
If <50- give 30 grams carbs

176
Q

Hypoglycemia protocol is patient cannot take PO

A

If awake: D5W 25mL IV push
If not awake:D5W 50mL IV push
No IV access- glucagon 1mg IM

177
Q

Inpatient glucose monitoring

A

Bedside POC method preferred
If receiving nutrition, check prior to any carbs
If not receiving nutrition check q 4-6 hrs
IV insulin- check every 30minutes- 2 hrs

178
Q

Enteral nutrition

A

Tube feed

179
Q

Parenteral nutrition

A

Through IV, TPN

180
Q

Glucocorticoid induced hyperglycemia

A

Elevated PPG BG

Glucocorticoids increase insulin resistance

181
Q

Glucocorticoid induced hyperglycemia treatment

A

Once daily prednisone and insulin naive-
NPH 0.1unit/kg for every 10mg prednisone
Once daily prednisone and at home insulin-
Add weight based total to normal basal insulin dose

Twice daily prednisone or dexamethasone- long acting insulin

182
Q

Does DKA or HHS have higher mortality?

A

HHS

183
Q

Diabetic ketoacidosis

A

Typically type 1 DM

Uncontrolled hyperglycemia causes increased ketone production which leads to a metabolic acidosis

184
Q

Hyperosmolar hyperglycemic state

A

Typically Type 2 DM

Severely high BG, dehydration, and hyperosmolality

185
Q

Counterregulatory hormones in DKA and HHS

A

All are increased
DKA- absolute insulin deficiency
HHS- relative insulin deficiency

186
Q

What is the most common precipitating factor for DKA?

A

Infection in known T1DM patients

Newly diagnosed T1DM

187
Q

Why do some women not take their insulin?

A

Hyperglycemia causes weight loss and insulin causes weight gain

188
Q

Clinical presentation of DKA

A

polyuria, polydipsia, weight loss, N/V, abdominal pain, dehydration, weakness, mental status changes, poor skin turgor , Kussmaul respirations, tachycardia, hypotension

189
Q

Kussmaul respirations

A

Pt has abnormal respirations because body is trying to blow off CO2
DKA

190
Q

Diagnostic features of DKA

A

Elevation in total blood ketone concentration
Ketones in urine- acetoacetate and acetone
Ketones in blood stream- beta-hydroxybutyrate

191
Q

MUDPILES

A 
Anion-gap metabolic acidosis
Methanol toxicity
Uremia
DKA
Paraldehyde toxicity
Infection
Lactic acidosis
Ethylene glycol toxicity
Salicylate toxicity
192
Q

Anion gap metabolic acidosis

A

Anything >10-12mEq/L

193
Q

Why do you check amylase and lipase in anion gap metabolic acidosis?

A

They are raised if the cause is pancreatitis

194
Q 
DKA findings:
pH-
Sodium bicarb-
Urine ketone-
Serum ketone-
Serum osmolality-
Anion gap-
Mental status-
A 
pH- <7.3 (more severe with lower pH)
Sodium bicarb- <18 (the lower the bicarb is the more severe)
Urine ketone-Positive
Serum ketone-Positive
Serum osmolality- Variable
Anion gap- >10-12
Mental status- Alert to coma in severe
195
Q 
HHS findings:
pH- 
Sodium bicarb-
Urine ketone-
Serum ketone-
Serum osmolality-
Anion gap-
Mental status-
A 
pH- >7. 3 (more normal)
Sodium bicarb- Normal (>18)
Urine ketone-  Small to none
Serum ketone- Small to none
Serum osmolality- >320mOsm/kg
Anion gap- Variable
Mental status-Stupor/coma
196
Q

Treatment goals of DKA and HHS

A

Correct dehydration, hyperglycemia, and electrolyte imbalances
Treat with fluids, insulin (treating acidosis!), and electrolytes

197
Q

Fluid therapy for treatment of DKA

A

Give 1-1.5 L in first hour 0.9% NaCl bolus immediately while waiting on labs.
If corrected Na normal or elevated- 0.45% NaCl at at rate of 250-500mL/hr
If corrected Na low- 0.9% NaCl at a rate of 250-500mL/hr

198
Q

When do you want to see correction in DKA?

A

Fluid deficit- w/in 24 hours
Hyperglycemia- w/in 6 hours
Ketoacidosis- w/in 12 hours (this is why you continue giving insulin past when the hyperglycemia is fixed)

199
Q

DKA dosing insulin therapy

A

Regular insulin
0.1units/kg bolus followed by a 0.1unit/kg/hour infusion
OR
0.14units/kg/hr infusion

You are not titrating insulin

Goal is to not drop glucose too quickly

200
Q

When do you reduce rate of insulin therapy in DKA?

A

When BG is 200mg/dL you reduce rate to 0.02-0.05units/kg/hr and give D5W
Goal BG 150-200mg/dL until resolution of DKA

201
Q

When do you give K with DKA?

A

If K <3.3
-Hold insulin and give K 20-30mEq/L until K >3.3

If K 3.3-5.2
-20-30mEq K/L of replacement fluid with insulin

If K > 5.2
Do not add K
Check serum K in 2 hours

202
Q

When do you give bicarb in DKA?

A

When pH <6.9 give 100mEq bicarb

203
Q

Criteria for resolution of DKA

A 
BG <200mg/dL
Two of the following:
Serum bicarb >15mEq/L
Venous pH >7.3
AG <12
204
Q

Criteria for resolution of HHA

A

Normal osmolality

Normal mental status

205
Q

Transition to SQ insulin after DKA

A

Make sure there is an overlap of 1-2 hours between discontinuation of insulin infusion and administration of SQ insulin

206
Q

Complications of treating DKA

A

Hypokalemia
Hypoglycemia (BG monitoring q 1-2h)
Hyperchloremia
Cerebral edema

207
Q

HHS causes

A

Typically in older adults due to restricted water intake.

It involves over days to weeks

208
Q

Energy balance

A

Energy intake- total energy expenditure

209
Q

TEE

A

resting metabolic rate (RMR) x physical activity level (PAL)

210
Q

Physical activity level

A

Sedentary- 1.2
Low to moderate- 1.4
Active- 1.6

211
Q

Carbohydrates

A

4 calories/gram

45-65% total calories

212
Q

Simple sugars

A

Fructose, fruits, milk (lactose)

Less than 10% calories/day added sugars

213
Q

Complex starches

A

Beans, peas, nuts, grains, starchy vegetables

214
Q

Complex fiber

A

Insoluble- helps maintain a healthy digestive system and regularity
Soluble- Helps control BG and cholesterol

14 grams of fiber for every 1,000 calories

215
Q

Protein

A

4 calories/gram
10-35% of total calories
0.8grams /kg/day of protein

Animal sources, plant s (soy, beans, nuts, quinoa

216
Q

Fat

A

9 calories/gram\

20-35% of total calories from fat

217
Q

Monounsaturated fatty acids

A

Healthy

Avocadoes, nuts, seeds, olive oil, canola oil, peanut oil

218
Q

Polyunsaturated fatty acids

A

Healthy

ALA, soy beans, walnuts, flax seeds, DHA/EPA, salmon and other seafood

219
Q

Trans fatty acids

A

margarines and processed foods

Unhealthy

220
Q

Saturated fatty acids

A

Unhealthy
Animal fat, coconut oil, palm oil, cocoa oil

Less than 10% of calories should come from fats

221
Q

Daily sodium recommendations

A

Less than 2300mg/day

222
Q

Alcohol

A

7 calories/gram

Up to 2 drinks for men and 1 for women per day

223
Q

Healthy eating plate

A

1/2 fruits and veggies
1/4 whole grains
1/4 healthy protein
skip sugary drinks

224
Q

Starches grams of carbohydrate per serving

A

15

225
Q

Fruits grams of carbohydrate per serving

A

15

226
Q

Milk grams of carbohydrate per serving

A

12

227
Q

Nonstarchy veggies grams of carbohydrate per serving

A

5

228
Q

Meat, proteins, and fats grams of carbohydrate per serving

A

0

229
Q

Women carb requirements

A

Need about 45-60 grams carbs at each of 3 meals and 15 grams for snacks prn

230
Q

Men carb requirements

A

Need 60-75 grams carbs at each 3 meals and 15-30 grams carbs for snacks prn

231
Q

Is there an ideal percentage of calories from carbs, proteins, and fat for people at risk for diabetes?

A

No

232
Q

ADA total dietary allowance of carbs for adults w/o diabetes

A

130g/day to fulfill brains requirement

233
Q

Two systematic reviews of the literature regarding GI and GL in individuals with diabetes report

A

No A1C impact

234
Q

Does the ADA support limiting carbs for the general population?

A

No

235
Q

Healthcare providers should focus on:

A

Emphasize nonstarchy veggies
Minimize sugars and refined grains
Choose whole foods over highly processed foods

Reduce carbs in pts with DM

236
Q

Weight management

A

In T2DM, 5% weight loss is recommended. Optimal outcomes are seen at 15% or more weight loss if feasible

237
Q

Diabetes remission

A

Maintenance of euglycemia or prediabetes level of glycemia with no meds for 1 year

238
Q

Excess alcohol consumption can lead to

A

Hyperglycemia

Alcohol in people with DM can inhibit gluconeogenesis and cause hypoglycemia

239
Q

Etiology of obesity

A

Imbalance between energy intake and energy expenditure over time

240
Q

Medications associated with weight gain

A 
Anticonvulsants/mood stabilizers 
Antidepressants
Beta blockers
antidiabetics
Atypical antipsychotics
Antihistamines
Corticosteroids
Hormonal contraceptives
241
Q

Leptin

A

Comes from fat cells and decreases appetite.

There is a leptin resistance in obesity.

242
Q

What does an increase in FFA cause?

A

An increase in insulin

-weight gain and insulin resistance

243
Q

Defining obesity

A

A state of excess body fat as determined by measures in adiposity
BMI is used but does not take into account fat free mass
Can take intraabdominal fat waist circumference

244
Q

BMI calculation

A

Weight in kg/height in m^2

245
Q

Normal BMI

A

18.5-24.9 kg/m^2

246
Q

Obesity BMI

A

> 30 kg/m^2

247
Q

Measuring waste circumference

A

Narrowest circumference in area between last rib and top of iliac crest
High risk
men >40
women >35

248
Q

Weight loss goals

A

Initial goal: 5-10% loss of baseline weight w/in 6 months
Create an energy deficit of 500-750kcal/day
Women- 1200-1500 kcal/day
Men- 1500-1800 kcal/day

249
Q

When would you consider medications in obesity?

A

BMI >30

BMI> 27 with at least 1 associated obesity related condition

250
Q

When would you consider metabolic surgery in obesity?

A

BMI >40

BMI >35 with obesity associated comorbid conditions

251
Q

When do you D/C medication for obesity?

A

In pregnancy

If the response is less than 5% after 3 months

252
Q

Phentermine

A

Approved for short term use
Controlled substance
MOA- NE releasing agent
Contraindications- anxiety disorders, heart disease, HTN, seizures, MAOI, pregnancy/breast feeding, hyperthyroidism, glaucoma, drug abuse, idiosyncrasy to symathomimetic amines

253
Q

Orlistat

A

Chronic use
Alli- OTC
Xencal- Rx

Pancreatic and gastric lipase inhibitor

Contraindications- chronic malabsorption syndrome, cholestasis, oxalate nephrolithiasis, pregnancy/breastfeeding

254
Q

Phentermine/Topiramate

A

Dose titration
MOA- GABA receptor modulation plus NE releasing
Chronic

255
Q

Naltrexone/Bupropion

A

BBW- suicidal ideation
Goal dose 2 tablets BID 32/360mg
Chronic
Reuptake inhibitor of Ne and dopamine; opioid antagonist

256
Q

Saxenda

A

Liraglutide
Chronic
GLP1 RA

257
Q

Metabolic surgery

A

Achieves superior glucose control and reduction in CV risk factors in obese patients with T2DM

258
Q

Metabolic surgery RYGB

A

Gastric bypass

Most favorable risk-benefit ratio

259
Q

Metabolic surgery VSG

A

30% of procedures
Excellent weight loss
Long term studies needed

260
Q

Metabolic surgery LAGB

A

19% of procedures

Greater risk of complications

261
Q

Metabolic surgery BPD-DS

A

2% of procedures
Most effective but least favorable risk-benefit profle
Consider if BMI >60

Therapeutics II (5 decks)

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